Gnaiger 2000 Transpl Int
|Gnaiger E, Kuznetsov AV, Rieger G, Amberger A, Fuchs A, Stadlmann S, Eberl T, Margreiter R (2000) Mitochondrial defects by intracellular calcium overload versus endothelial cold ischemia/reperfusion injury. Transpl Int 13:555-7.|
Abstract: Questions as to the critical stress factor and primary targets of cold ischemia/reperfusion (CIR) injury were addressed by comparing mitochondrial defects caused by (1) CIR injury and (2) intracellular Ca2+ overload. CIR was simulated in transformed human umbilical vein endothelial cell cultures (tEC) by 8 h cold anoxia in University of Wisconsin solution and reoxygenation at 37 °C. Intracellular Ca2+ concentrations were changed by permeabilization of suspended cells with digitonin in culture medium (RPMI, 0.4 mM Ca2+). Binding of free Ca2+ by ethylene glycol-bis(β-aminoethylether)- N,N,N',N'-tetraacetic acid in RPMI or mitochondrial incubation medium served as controls. Extracellular Ca2+ protected the cell membrane against permeabilization. Mitochondrial functions were determined before and after permeabilization of the cell membrane. After CIR, mitochondrial respiratory capacity declined, but oxygen consumption remained coupled to adenosine triphosphate (ATP) production. In contrast, Ca2+ overload caused uncoupling of mitochondrial respiration. High intracellular Ca2+ overload, therefore, does not reproduce cold ischemia/ reperfusion injury in endothelial cells.
• Keywords: Ischemia/reperfusion injury, Endothelial cells, Plasma membrane, Intracellular Ca2+, Mitochondrial respiratory chain, Oxidative phosphorylation
Labels: MiParea: Respiration
Stress:Ischemia-reperfusion, Oxidative stress;RONS Organism: Human Tissue;cell: Endothelial;epithelial;mesothelial cell, HUVEC Preparation: Intact cells, Permeabilized cells, Oxidase;biochemical oxidation
Regulation: Calcium Coupling state: ROUTINE, OXPHOS